Clinical depression is a risk factor for mortality and morbidity after acute myocardial infarction (MI), yet little is known about the underlying mechanisms that account for this. The purpose of this study is to examine a potential mechanism, cardiovascular response to disordered sleep. Three months after an MI, 75 patients who meet the DSM-IV criteria for major depression will be selected and matched for gender, age, BMI to patients without depression. Polysomnography will be performed to determine the frequency and severity of cardiac responses to sleep disordered breathing and sleep architecture measures. The following hypotheses will be tested: 1) patients with depression have greater cardiac response to episodes of sleep apnea than non-depressed patients; 2) patients with depression without sleep disordered breathing have shorter REM latency, increased REM density, reduced slow wave sleep and worse sleep efficiency; 3) increased cardiac response to sleep disordered breathing, a shorter REM latency, increased REM density, decreased slow wave sleep are associated with electro cardio-graphic abnormalities predictive of cardiac events in post MI patients.